2018
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Browsing 2018 by Author "Aftabizadeh, Som"
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Item A Rare Case of Superior Vena Cava Syndrome caused by long-term indwelling Hemodialysis Catheter Placement(2018-03-14) Aftabizadeh, Som; Iyamu, Ikponmwosa; Nguyen, Thao; Madhrira, Machaiah; Reddy, Prashanth; Patel, AmanTitle: A Rare Case of Superior Vena Cava Syndrome caused by long-term indwelling Hemodialysis Catheter Placement First Authors: Dr. Som Aftabizadeh, DO, PGY-1 Co-authors: Dr. Thao Nguyen, DO, PGY-2; Dr. Aman Patel, DO, PGY-3; Dr. Prashanth Reddy, MD, PGY-1 Attendings: Dr. Ikponmwosa Iyamu, MD; Dr. Machaiah Madhrira, MD; Dr. Balamurugan Sankarapandian, MD Name of Institution- Medical City Fort Worth Name of institutional department, division or other administrative unit- Internal Medicine City, State, Zip Code: Fort worth, Texas, 76104 Background/Abstract: End-stage renal disease (ESRD) cases continue to rise at approximately 21,000 cases per year in the US.1 During the past decade there has been a trending increase in use of central venous catheters (CVC) for hemodialysis (HD).2-3 When inserted into the superior vena cava (SVC), these catheters have been shown to be associated with thrombosis. While malignancy is the most common cause of superior vena cava syndrome (SVCS), an increasing incidence of benign causes are appearing. A portion of these benign causes are associated with the increasing use of intravascular catheters.2,4 Case Report: A 51-year-old african american female with past medical history of ESRD on HD, type II diabetes mellitus, coronary artery disease, paroxysmal atrial fibrillation who presented to our emergency department with acute neck swelling associated with hoarseness and headache. She states she woke up on the morning of admission with diffuse bilateral neck swelling that increased in size throughout the day. She denied difficulty with swallowing solids or liquids. She also denied difficulty with respiratory effort, chest pain, or shortness of breath. Her Vitals were stable. Clinical exam showed minimal facial edema but prominent superficial veins of the chest wall and neck region. Chest x-ray showed widening of the mediastinum. Our initial clinical impression was cellulitis, angioedema, or allergic reaction. Chest CT showed a thrombus partially occluding the SVC with severe stenosis at the cavoatrial junction. The patient was diagnosed with SVCS and underwent recanalization with angioplasty and stenting of SVC. The symptoms of superior vena cava syndrome began to improve immediately after the angioplasty and she continued to be free of symptoms and was subsequently discharged home. Of note, the patient had a long history of CVC access with repeated and prolonged placement after failed AVGs. Discussion/Conclusion: SVC syndrome is a medical emergency and can be fatal if resulting in severe cerebral edema and cerebellar herniation. A slower development of SVC is often better tolerated as many patients develop collateralization of vessels.4 It is thought that approximately half of central vein stenosis remain asymptomatic with clinical manifestations presenting due to eventual local upstream hypertension. In addition to risk of thrombosis of all CVCs, hemodialysis related CVCs are believed to have increased risk of thrombosis due to having longer, thicker lumens and longer length of placement.5-6 Therapy is generally endovascular or surgical with the former fairing better in hemodialysis patients with multiple comorbidities.7 This case illustrates the unusual manner in which SVC can present along with the potential for iatrogenic causes of SVC syndrome. Given the increasing frequency of intravascular catheter placement, it’s important to identify iatrogenic causes. Avoiding long term use of hemodialysis catheters and timely creation of AVFs may help prevent these complications. References: Lok CE, Foley R. Vascular access morbidity and mortality: trends of the last decade. Clin J Am Soc Nephrol. 2013;8(7):1213-9. A rare complication of hemodialysis catheters: superior vena cava syndrome. Akoglu H, Yilmaz R, Peynircioglu B, Arici M, Kirkpantur A, Cil B, Altun B, Turgan C Hemodial Int. 2007 Oct; 11(4):385-91. Warren P, Burke C. Endovascular management of chronic upper extremity deep vein thrombosis and superior vena cava syndrome. Semin Intervent Radiol. 2011;28(1):32-8. https://emedicine.medscape.com/article/460865-overview Quaretti P, Galli F, Moramarco LP, et al. Dialysis catheter-related superior vena cava syndrome with patent vena cava: long term efficacy of unilateral Viatorr stent-graft avoiding catheter manipulation. Korean J Radiol. 2014;15(3):364-9. Seelig MH, Oldenburg WA, Klingler PJ, Odell JA. Superior vena cava syndrome caused by chronic hemodialysis catheters: autologous reconstruction with a pericardial tube graft. J Vasc Surg. 1998;28(3):556-60. https://emedicine.medscape.com/article/460865-treatmentItem An Unusual Case of Viral Cardiomyopathy Presenting as Acute Ischemic CVA(2018-03-14) Aftabizadeh, Som; Walji, Shaista; Chennupati, Anupama; Nguyen, ThaoBackground/Abstract: HIV HIV-associated cardiomyopathy (HIVAC) is a significant cause of morbidity and mortality among HIV-infected individuals.1 The HIV virus is increasingly becoming recognized as an important cause of cardiomyopathy. While the exact mechanism remains unclear, effects from direct viral burden as well as opportunistic infections are thought to play a key role.2 Here we present a case of severe cardiomyopathy in a patient previously undiagnosed with HIV. Case Report: A 21yo Hispanic male with PMH significant for fatty liver disease and recent Tylenol toxicity presented to the ER for evaluation of sudden onset of left sided weakness and left facial droop. He was found down and noted to be shaking, thus there was also a concern for seizure activity. NIHSS upon arrival was 16, with early changes on CT and visualized clot in M1 distribution of the right MCA with poor collateral flow on CTA. Right MCA syndrome was diagnosed and patient was given tPA. Patient recovered well with rapid resolution of the focal deficits. Prothrombotic workup revealed low protein C activity. Transthoracic echo performed as part of evaluation of ischemic CVA demonstrated a LVEF of 15% and moderately dilated left ventricle.. The etiology of CVA was felt to be thromboembolic secondary to this severe cardiomyopathy. Patient denied any personal or family history of prior cardiac problems as well as cardiac arrhythmias. Due to noted recurrent fevers and pancytopenia throughout the course of his admission, HIV reactivity was checked and revealed him to not only have HIV but also AIDS with a CD4 count of 84 and RNA PCR of 121,000. With this finding, viral cardiomyopathy was felt to be the most reasonable explanation for heart failure in this young patient. He was started on oral anticoagulation to prevent further thromboembolic events and was fitted for a LifeVest. Discussion/Conclusion: HIV- associated cardiomyopathy is a known chronic complication in patients living with HIV/ AIDS, especially in uncontrolled infection as was seen in the patient who presented to our hospital. Uncontrolled infection can lead to both direct and indirect cardiotoxicity from infections associated with low CD4 counts as well as HIV itself. The pathogenesis of HIV- induced cardiomyopathy is often multifactorial including myocarditis, cardiac autoimmunity, micronutrient deficiency, and even antiretroviral therapy (ART) induced.1 Patients living with HIV are at a higher risk than the general population for developing HF. Studies have shown that in HIV-infected individuals, the prevalence of HF was highest among those with CD4 counts References: Lumsden RH, Bloomfield GS. The Causes of HIV-Associated Cardiomyopathy: A Tale of Two Worlds. Biomed Res Int. 2016;2016:8196560. Al-kindi SG, Elamm C, Ginwalla M, et al. Heart failure in patients with human immunodeficiency virus infection: Epidemiology and management disparities. Int J Cardiol. 2016;218:43-46. Ntsekhe M, Mayosi BM Cardiac manifestations of HIV infection: an African perspective. Nat Clin Pract Cardiovasc Med. 2009;6:120–127. Gopal M, Bhaskaran A, Khalife WI, Barbagelata A. Heart Disease in Patients with HIV/AIDS-An Emerging Clinical Problem. Curr Cardiol Rev. 2009;5(2):149-54. Currie PF, Jacob AJ, Foreman AR, Elton RA, Brettle RP, Boon NA. Heart muscle disease related to HIV infection: prognostic implications. BMJ. 1994;309:1605–1607. Felker GM, Thompson RE, Hare JM, Hruban RH, Clemetson DE, Howard DL, Baughman KL, KasperEK. Underlying causes and long-term survival in patients with initially unexplained cardiomyopathy.N Engl J Med. 2000;342:1077–1084Item Neuroleptic Malignant Syndrome caused by Cyclobenzaprine(2018-03-14) Aftabizadeh, Som; Patel, Harsh; Herekar, Amar; Machaiah, Madhrira; Reddy, PrashanthBackground/Abstract: Neuroleptic malignant syndrome is a disorder characterized by a triad of fever, muscle rigidity and altered mental status and classically associated with dopamine antagonists. It is rare and potentially fatal if not diagnosed and treated in the correct manner. There is no specific diagnostic test to rule in the disorder and a high suspicion and detailed list of home medications are needed as it is essentially a clinical diagnosis. A patients course usually begins with muscle rigidity followed by a fever within several hours, as well as mental status changes that range from drowsiness, agitation, or confusion to a severe delirium or coma. Here we present a unique case of a patient with NMS secondary to cyclobenzaprine. To our knowledge, it is only the third case reported in literature.1-3 Case Report: A 70 year old male with a past medical history of left-sided ischemic stroke, hypertension, type II diabetes, and chronic back pain presented to our emergency department with altered mental status (AMS). His last known normal was the previous evening around 10pm where the wife admitted to a verbal argument over the patient’s frequent overuse of prescribed Norco and Flexeril for his chronic back pain. Upon waking up the following morning the patient’s wife immediately noticed AMS, unsteady gait, and loss of bladder control. Upon arrival to our ED the patient was febrile with a max temperature of 104.9, profusely diaphoretic, tachypneic, tachycardic, with muscle rigidity. Pupils were equal and reactive and reflexes were intact. The patient’s altered mentation and labored breathing continued to decline requiring intubation and mechanical ventilation. Computed tomography and magnetic resonance imaging of the brain were normal. Continuous EEG was negative for seizure activity. CSF analysis, blood, and urine cultures were negative for infection. Creatine kinase was elevated at 1,963 U/L and WBC elevated at 21.9 k/mm3. Urine triage screen was positive for opiates. The patient was treated with dantrolene and lorazepam with good response in temperature. Slowly, over the course of the next few days, the patient’s symptoms resolved and he was weaned of the ventilator and eventually discharged with no complications. Discussion/Conclusion: Our patient’s clinical presentation and diagnostic work-up were classic for NMS. Treatment is largely supportive including cessation of the offending agent and pharmacologic interventions in more severe cases such as ours. NSM is thought to be caused by abrupt dopamine receptor blockage and the typical causative agents are antipsychotics. NMS caused by cyclobenzaprine is extremely rare and to the best of our knowledge only two other case reports have been reported in literature. While our case points to an overdose as the most likely pathogenesis, other reports have described a possible idiosyncratic reaction, i.e., immune-mediated reactions that occur rarely and in unpredictable fashion among the population. This case questions if medications other than antipsychotics such as muscle relaxers should be kept in mind when working up a cause for NMS. The fact that a muscle relaxant can actually potentiate muscle rigidity makes this a unique phenomenon and we feel it should be further investigated. References: Berman BD. Neuroleptic malignant syndrome: a review for neurohospitalists. Neurohospitalist. 2011;1(1):41-7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3726098/ http://journal.chestnet.org/article/S0012-3692(16)53939-7/fulltext Fink M. Response to "Neuroleptic malignant-like syndrome due to cyclobenzaprine?". J Clin Psychopharmacol. 1996;16(1):97-9. https://emedicine.medscape.com/article/816018-overview#a4Item S1Q3T3 Leading to Early Suspicion of Pulmonary Embolism in Low-Risk Patient(2018-03-14) Reddy, Prashanth; Patel, Harsh; Machaiah, Madhrira; Thambidorai, Senthil; Mughal, Iqbal; Ahsan, Syed; Aftabizadeh, SomBackground/Abstract: Acute pulmonary embolism (PE) may prove fatal without early suspicion and subsequent treatment. Many cases go undiagnosed, with one study showing an estimated 70% of post mortem PE cases were undiagnosed at the time of death.1 Young patients are most at risk of being misdiagnosed as suspicion in this population is very low. Even with a variety of diagnostic modalities a high clinical suspicion remains key for diagnosis.2 The varying degree of clinical presentation makes diagnosing PE very difficult. Here we present a case of a patient with no known risk factors and WELLS score of 0 whose electrocardiogram (EKG) findings led to an early investigation, diagnosis, and subsequent treatment of a massive pulmonary embolism. Case Report: A 34 year old AAM with a PMHx of asthma presented to our ED with a chief complaint of substernal chest pain with associated dyspnea. On arrival, the patient was hemodynamically stable with all VS in normal range. CXR showed no acute process. Our team was called to admit the patient from the ED for uptrending troponins and an EKG with inferior lead T-wave inversions. Troponins trended up to 0.255. His EKG showed sinus tachycardia with T-wave inversion in inferior and anterior leads along with S wave in lead I and Q wave in lead III. WELLS score was 0. Though not sensitive, the EKG findings increased our suspicion for PE. D-dimer was ordered and found to be elevated at 6,693. A stat Chest CTA revealed a large saddle pulmonary emboli. LMWH therapy was initiated. Work-up for genetic and acquired factors were negative and patient was discharged on oral anticoagulation. Discussion/Conclusion: EKG findings in patients with PE have been a topic of much debate since first reports of investigation in 1935. Over the years medicine has evolved with ubiquitous access to more effective modalities for diagnosing PE. Despite the advent of these other modalities, the diagnosis of PE remains elusive and the prognosis is variable depending on clinical presentation and appropriate diagnosis and treatment.4 While the S1Q3T3 pattern is commonly taught in medical schools around the world as the pathognomonic ECG pattern associated with pulmonary embolism, its reported incidence in acute PE is highly variable with studies showing its incidence anywhere from 10-50%.5 Non-specific ST elevation and T wave inversion in inferior and anterior precordial leads are the most frequently noted EKG abnormalities in patients presenting with acute PE.6 Acute pulmonary embolism in young males without risk factors is rare. Given the time sensitive nature of appropriate diagnosis and treatment of PE, it is important that health care providers recognize EKG findings characteristic of PE. These findings can incite suspicion in low risk patients and direct subsequent work-up and management in a timely fashion.